This study explored the regulatory role of microRNA-1271 (miR-1271) in glioblastoma multiforme (GBM) proliferation and invasion via calcium/calmodulin-dependent protein kinase 2 (CaMKK2). MiR-1271 and CaMKK2 expression were quantified in normal human astrocyte cells, GBM cell lines, and low- and high-grade glioma tissues. MKI67 expression in GBM cells was measured using quantitative real-time polymerase chain reaction. The target relationship between miR-1271 and the CAMKK2 gene was confirmed using the luciferase reporter assay. MTT and Transwell assays were used to analyze the role of miR-1271 and CAMKK2 in cell proliferation and invasion. Finally, CaMKK2 expression and AKT phosphorylation were detected by western blotting. MiR-1271 was significantly downregulated in high-grade glioma tissues and GBM cell lines. Conversely, CAMKK2 mRNA expression was upregulated in high-grade glioma tissues and GBM cell lines. We observed that miR-1271 directly targeted the 3′-untranslated region of CAMKK2, indicating an inverse relationship with miR-1271. Overexpressing miR-1271 inhibited GBM cell proliferation and invasion, whereas inhibiting miR-1271 increased cell proliferation and invasion. Silencing CAMKK2 expression also inhibited GBM cell proliferation and invasion. Furthermore, overexpressing miR-1271 inhibited AKT phosphorylation and MKI67 mRNA expression by targeting CAMKK2. These results indicate that miR-1271 regulates GBM cell proliferation and invasion, and that these effects involve directly targeting the CAMKK2 gene. Therefore, miR-1271 may serve as a new therapeutic target for developing GBM treatments.

这项研究探讨了microRNA-1271（miR-1271）在胶质母细胞瘤（GBM）增殖和通过钙/钙调蛋白依赖性蛋白激酶2（CaMKK2）侵袭中的调控作用。在正常人星形胶质细胞细胞，GBM细胞系以及低度和高度神经胶质瘤组织中，对MiR-1271和CaMKK2的表达进行了定量。使用定量实时聚合酶链反应测量GBM细胞中的MKI67表达。miR-1271和CAMKK2基因之间的靶标关系已通过荧光素酶报告基因检测法得以证实。使用MTT和Transwell分析来分析miR-1271和CAMKK2的作用在细胞增殖和侵袭中。最后，通过蛋白质印迹检测CaMKK2表达和AKT磷酸化。在高级神经胶质瘤组织和GBM细胞系中，MiR-1271显着下调。相反，在高级神经胶质瘤组织和GBM细胞系中，CAMKK2 mRNA表达上调。我们观察到miR-1271直接靶向CAMKK2的3'-非翻译区，表明与miR-1271呈反比关系。过表达miR-1271抑制GBM细胞增殖和侵袭，而抑制miR-1271则增加细胞增殖和侵袭。沉默CAMKK2表达也抑制了GBM细胞的增殖和侵袭。此外，过度表达的miR-1271抑制AKT磷酸化和MKI67靶向CAMKK2的mRNA表达。这些结果表明，miR-1271调节GBM细胞的增殖和侵袭，并且这些作用涉及直接靶向CAMKK2基因。因此，miR-1271可以作为开发GBM治疗的新治疗靶标。